Abstract
Ischemia and reperfusion lead to the activation of circulating leukocytes with ensuing accumulation, aggregation, and adhesion to the endothelium of postcapillary venules. Through the release of inflammatory mediators and cytotoxic enzymes and the formation of oxygen free radicals adherent leukocytes contribute to reperfusion injury [1, 2]. Therapeutic approaches such as leukocyte depletion by antineutrophil serum or blockage of leukocyte adhesion by monoclonal antibodies have been shown effectively to improve the outcome of reperfusion injury [3, 4]. Adenosine exerts several anti-inflammatory actions by the inhibition of oxygen free radical formation, release of inflammatory mediators, and leukocyte adherence to cultured endothelial cells [5–7]. These effects are mediated via interaction with the adenosine A2 receptor [5].
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© 1993 Springer-Verlag, Berlin Heidelberg
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Nolte, D., Lehr, H.A., Messmer, K. (1993). Adenosine Inhibits Postischemic Leukocyte Adherence to the Endothelium of Postcapillary Venules via A2 Receptor. In: Faist, E., Meakins, J.L., Schildberg, F.W. (eds) Host Defense Dysfunction in Trauma, Shock and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77405-8_45
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DOI: https://doi.org/10.1007/978-3-642-77405-8_45
Publisher Name: Springer, Berlin, Heidelberg
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